Search In this Thesis
   Search In this Thesis  
العنوان
The possible protective effect of ACE2 activator “diminazene aceturate” and ACE inhibitor “ENALAPRIL” on acute myocardial infarction in rats/
المؤلف
El Naggar, Asmaa Samy Farag.
هيئة الاعداد
باحث / أسماء سامي فرج عبد اللطيف النجار
مناقش / آمال حسين برهامي
مناقش / سميحة محمود السيد
مشرف / أدهم راشد محمد
الموضوع
Physiology.
تاريخ النشر
2018.
عدد الصفحات
96 p.:
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الطب (متفرقات)
تاريخ الإجازة
24/4/2018
مكان الإجازة
جامعة الاسكندريه - كلية الطب - Medical Physiology
الفهرس
Only 14 pages are availabe for public view

from 124

from 124

Abstract

The renin angiotensin system (RAS) plays a critical role in maintaining cardiovascular homeostasis. ACE and its novel homolog ACE2 are two key enzymes involved in the synthesis of bioactive components of the RAS. Activity of the ACE and ACE2 provides the basis for the presence of a counter-regulatory mechanism within the RAS. While ACE/Ang II/AT1R is a well-established axis of the RAS leading to vasoconstrictive, proliferative and proinflammatory effects, the ACE2/Ang-(1-7) /Mas receptor axis provides a vasoprotective, anti-proliferative and anti-inflammatory mechanism representing a counter-regulatory axis within the RAS.
Myocardial infarction (MI) is a cardiovascular pathological condition caused by imbalance between myocardial oxygen supply and demand causing myocardial necrosis, so that MI has been considered as one of cardiovascular diseases standing behind ventricular remodeling and cardiac dysfunction as MI can weaken cardiac contractility and consequently reduces stroke volume and cardiac output. Isoproterenol (ISO) is a sympathomimetic β-adrenergic receptor agonist which causes severe stress to the myocardium resulting in infarct like necrosis of heart muscle by several mechanisms mainly functional hypoxia, ischemia, changes in electrolyte contents and oxidative stress. ISO induced MI in rats is the model used in the current study as it is considered to be a widely-accepted model to investigate the molecular mechanism behind left ventricle dysfunction and remodeling.
Ventricular remodeling post-MI is initiated by neurohormonal activation, myocardial stretch and the activation of the local tissue RAS. Ang II is considered as an important mediator of myocardial remodeling, leading to impairment of cardiac function, and represents an important risk factor for heart failure in experimental models and patients. While Ang-(1-7) has been shown to have a protective effect against Ang II induced cardiac hypertrophy and remodeling.
It was demonstrated that RAS inhibition may reverse post-infarction remodeling due to hemodynamic unloading, neuroendocrine modulation, or its direct effects on the remodeling myocardium. Enalapril is one of the ACE inhibitors which prevents further deterioration of cardiac performance and improves clinical outcome. It is also used in treatment of heart failure due to its cardioprotective effect in prevention of further deterioration of ventricular function, reduction of reperfusion injury, infarct size, reperfusion arrhythmias and other ventricular arrhythmias.